HISTORY AND PHYSICAL EXAMINATION = DIAGNOSIS

A doctor who cannot take a good history and a patient who cannot give one are
in danger of giving and receiving a bad treatment
Goals of History Taking :
1. Gaining the patients confidence
2. Assessing the personality and character of the patient
3. Arriving at a tentative diagnosis
4. Plotting the work-up
The greater the number of symptoms , the less significance of each
Psychosomatic reaction / PPSR ? or Neurocirculatory asthenia ?
Sign and Symptoms of Cardiac Diseases :
Shortness of breath ( dyspnea )
Orthopnea, easy fatigability, PNDs
Swelling of the feet and enlarging abdomen / ascites ( edema )
Pain in the chest ( angina ) : LPPQRST localization, precipitating,
palliative , quality, radiation, severity, timing/ temporal profile
Palpitations
Cyanosis ( central/ peripheral type ), clubbing
Hemoptysis ; nocturia , loss of appetite, nausea, vomiting ; abdominal
pain, dysphagia ; dizziness / syncope ; visual disturbances ; epistaxis ;
skin/ dry/ sweating/pale / flushed
PAST HISTORY : DM , thyroid disease or other metabolic disorders ? ;
rheumatic fever, occupation , exposure to cardiotoxic agents , has he taken any
cardiac meds, digitalis . What is the tobacco or alcohol history ? Cocaine /
methamphetamine / shabu use ? has she been taking the pill ?
FAMILY HISTORY : any close member with congenital heart dse, RF, DM, HPN,
or CAD ? anybody died at an earlier age from IHD or HPN
PHYSICAL EXAMINATION
directed history and a targeted physical examination
clinical performance does not improve predictably as a function of experience;
instead, the acquisition of new examination skills may become more difficult for a
busy individual practitioner
Educational techniques to improve bedside skills include repetition, patientcentered teaching conferences, and visual display feedback of auscultatory
events with Doppler echocardiographic imaging
Why do we need to do physical examination ?
history and physical examination to the presence, severity, and prognosis of
cardiovascular disease

heart rate, blood pressure, signs of pulmonary congestion, and the presence of
mitral regurgitation (MR) bedside risk assessment in patients with acute
coronary syndromes
can inform clinical decision making before the results of cardiac biomarkers
testing are known.
jugular venous pressure (JVP) and the presence or absence of a third heart
sound (S3) prognosis of patients with systolic heart failure
Accurate characterization of cardiac murmursvalvular and congenital heart
lesions
enhancing the clinician-patient relationship cannot be overestimated

GENERAL APEARANCE :
The examination does not wait until the removal of the shirt .

general appearance of the patient, with notation of age, posture,

demeanor, and overall health status
in pain or resting quietly, dyspneic or diaphoretic
avoid certain body positions to reduce or eliminate pain, as might be the
case with suspected acute pericarditis
pulmonary cause increased anterior-posterior diameter, tachypnea, and
pursed-lip breathing
Skin pallor, cyanosis, and jaundice

1. Stroke: face, limb , gait possibilities : atrial fibrillation, myocardial infarction,

or infective endocarditis ( IE ) ; in the young MVP, MS, atrial myxoma ,
Lupus erythematosus ; in the older group : hypertension, IE , prosthetic valve
2. Obesity : Pickwickian syndrome with RV failure
a) BMI = wt ( kg) / m 2 normal : 20 to 23 ; overweight : 23.1 to 28 ;
obese class I :28.1 to 35 ; obese class II : > 35
b) Waist circumference : < 34 inches ( 90 cm ) for male
> 30 inches ( 80 cm ) for female
3. Wide based gait and slapping feet : tabes dorsalis aortic syphilitic dse.
4. Marfans syndrome: long arms producing a span greater than the height ,
tremulous iris , arachnodactyly dissecting aneurysm
5. Pericarditis : not dyspneic and leaning forward
PHYSICAL EXAMINATION
Central cyanosis often assoc. with clubbing ; right to left cardiac or
extracardiac shunting or inadequate oxygenation of blood by the lungs
Peripheral cyanosis peripheral vessel involvement / obstruction of
venous return or due to arterial occlusion or vasospasm
Differential cyanosis - isolated cyanosis affecting the lower but not the
upper extremities in a patient with a large patent ductus arteriosus (PDA)
and secondary pulmonary hypertension with right-to-left to shunting at the
great vessel level

SKIN :
hemochromatosis : unusually tan or bronze discoloration ; cause of the
associated systolic heart failure
Jaundice : visible first in the sclerae, has a broad differential diagnosis but
in the appropriate setting can be consistent with advanced right heart
failure and congestive hepatomegaly or late-term "cardiac cirrhosis
Cutaneous ecchymosis : vitamin K antagonists or antiplatelet agents such
as aspirin and thienopyridines
Lipid disorders : subcutaneous xanthomas, particularly along the tendon
sheaths or over the extensor surfaces of the extremities
Severe hypertriglyceridemia can be associated with eruptive
xanthomatosis and lipemia retinalis.
Palmar crease xanthomas : specific for type III hyperlipoproteinemia
Pseudoxanthoma elasticum, a disease associated with premature
atherosclerosis, is manifested by a leathery, cobblestoned appearance of
the skin in the axilla and neck creases and by angioid streaks on
funduscopic examination.
Extensive lentiginoses : Carney syndrome, which includes multiple atrial
myxomas.
lupus pernio and erythema nodosum dilated cardiomyopathy, especially
with heart block, intraventricular conduction delay, or ventricular
tachycardia
HEAD :
De Musset sign : head bobbing in Aortic Regurgitation
Enlarged skull : Pagets disease ; increased pulse pressure ( SBP- DBP =
> 40 mm Hg ) ; high output failure due to arteriovenous fistulae in affected
bones?
Premature frontal baldness : CAD ?
Osler-Weber-Rendu syndrome (hereditary hemorrhagic telangiectasia):
Hereditary telangiectasias on the lips, tongue, and mucous membranes
Malar telangiectasia : mitral stenosis and scleroderma
High arched palate : Marfans syndrome and other connective tissue
disease
Bifid uvula : Loeys-Dietz syndrome
Orange tonsils :Tangier disease
Congenital heart diseases : associated hypertelorism, low-set ears, or
micrognathia.
FACE :
Myxedema : coarse , puffy face , dry sallow skin, sparse eyebrows
pericardial effusion, CHF , CAD and mild HPN
Thyrotoxicosis : exopthalmos, lid lag atrial fibrillation and high output
failure ; MVP
Hypothyroidism CHF

Mitral facies rosy malar prominences with peripheral cyanosis

Butterfly rash disseminated lupus pericarditis, myocarditis,
verrucous endocarditis
Carcinoid syndrome : brick red cyanosis ; damage to right side valves ;
PS and TR ; due to circulating serotonins; paroxysmal flushing
Jaundice : Tricuspid valve dse. , cardiac cirrhosis, pulmonary infarction
and hemolysis caused by prosthetic valve
Downs syndrome : ASD or endocardial cushion defect
Supravalvular AS puckish face poorly developed lower jaw , thick lips ,
wide set eyes , low set ears, retarded but impish look

EYES :
Arcus senilis or coneal arcus : under the age of 50 y/o hyperlipidemia
or early atherosclerosis ? ; lacks specificity as an index of coronary heart
disease risk.
Xanthelasma / Xanthomas lipid deposits
Cataract : DM ? ; in the young : rubella syndrome PDA
Blue sclerae : osteogenesis imperfect
Fundoscopy : assess the microvasculature, especially among patients
with established atherosclerosis, hypertension, or diabetes mellitus ;
should be performed routinely in the assessment of patients with
suspected endocarditis and those with a history of acute visual change ;
Branch retinal artery occlusion or visualization of a Hollenhorst plaque
Relapsing polychondritis may manifest as an inflamed pinna or, in its later
stages, as a saddle-nose deformity because of destruction of nasal
cartilage
Wegener's granulomatosis can also lead to a saddle-nose deformity.
Examination of the Retina
Arteriovenous ratio ; Optic disc: edema ; blurred margins cupping with
sharp contours ; Keith Wageners classification ( See Barbara Bates
book )
Variations of caliber : beading ; hypercholesterolemia or spasm ;
Severe HPN : scattered flame- shaped hges , very constricted arterioles,
cotton wool spots;
Hollenhurst cholesterol plaques and calcium emboli : from the heart , aorta,
great vessels or carotid arteries
EARS :
Pulsatile ears TR
Diagonal crease : assoc. with CAD but does not apply to Native American
Indians

NECK :
Vigorous carotid arterial pulsations AR , coarctation of the aorta (COA),
thyrotoxicosis or anxiety
Distended veins : RV failure , tricuspid valve dse, SVC syndrome
Webbed neck : Turners syndrome ( infantilism) COA
Noonans syndrome : ( short stature , webbed neck , hypertelorism,
mental and sexual retardation) PS ; often with ASD
CHEST :
COPD: pink puffer / blue bloater ( emphysema/ chronic bronchitis ,
respectively ) cor pulmonale , RV failure
Barrel chest deformity , pursed lips , tachypnea and use of accessory
muscles COPD
Kyphoscoliosis cor pulmonale
Cheyne stoke respiration : ( wax and wane respiration separated with
apneic spells ) serious cardiovascular and cerebrovascular disease ;
LV failure
Midline sternotomy, left posterolateral thoracotomy, or infraclavicular scars
at the site of pacemaker/defibrillator generator implantation
subclavian or vena caval obstruction : prominent venous collateral pattern
: head and neck appear dusky and slightly cyanotic and the venous
pressure is grossly elevated without visible pulsations SVC syndrome
Connective tissue disease : pectus carinatum ("pigeon chest") and pectus
excavatum ("funnel chest")
severe kyphosis and compensatory lumbar, pelvic, and knee flexion of
ankylosing spondylitis Aortic regurgitation
Straight back syndrome refers to the loss of the normal kyphosis of the
thoracic spine and has been described in patients with mitral valve
prolapse (MVP) and its variants
cyanotic congenital heart disease, the chest wall appears to be
asymmetric, with anterior displacement of the left hemithorax
HANDS :
Hyperthyroidism : warm , sweaty palm tachycardia can cause
Cardiomyopathy
Hypothyroidism : rough , dry skin bradycardia can cause
Cardiomyopathy
Clubbing : congenital cardiac or pulmonary disease ; central right to left
shunts and also infective endocarditis ; cyanosis and softening of the root
of the nail bed, to the classic loss of the normal angle between the base of
the nail and the skin, to the skeletal and periosteal bony changes of
hypertrophic osteoarthropathy, which is seen rarely in patients with
advanced lung or liver disease
Splinter hemorrhages : linear petechiae under the nail ( midposition of the
nail beds ) may be the first clue in IE esp with a patient with FUO ; but
can also be seen in minor trauma ; high altitudes

Janeway lesions of endocarditis are non-tender, slightly raised

hemorrhages on the palms and soles, whereas Osler's nodes are tender,
raised nodules on the pads of the fingers or toes
Polydactyly of Ellis Van Creveld dwarfism or the fingerized thumb of the
Holt Oram syndrome ASD
Scleroderma - tight shiny skin myocardial fibrosis and necrosis
secondary to coronary involvement
Marfans syndrome : arachnodactyly and a positive "wrist" (overlapping of
the thumb and fifth finger around the wrist) or "thumb" (protrusion of the
thumb beyond the ulnar aspect of the hand when the fingers are clenched
over the thumb in a fist) sign
Lower extremity or presacral edema in the setting of an elevated JVP
defines volume overload and may be a feature of chronic heart failure or
constrictive pericarditis

EXAMNATION OF THE ABDOMEN

Abdominal aorta : aortic aneurysm ; pulsatile abdominal mass
CHF or constrictive pericarditis : enlarged tender liver
TR : systolic hepatic pulsation
Severe CHF / IE : palpable spleen
Ascites
Arteriovenous fistula : continuous murmur
Renal artery stenosis : systolic bruit over the kidneys
Significant TR : Systolic pulsations over the liver
Splenomegaly may be a feature of infective endocarditis
Ascites :nonspecific finding but may be present with advanced chronic
right heart failure, constrictive pericarditis, hepatic cirrhosis, or an
intraperitoneal malignancy

EXAMINATION OF THE EXTREMITIES

Palpate lower and upper extremities pulses ( DP, PT, P, F, B, R )
Edema
clubbing, arachnodactyly, and pertinent nail findings
Muscular atrophy or the absence of hair along an extremity is consistent
with severe arterial insufficiency or a primary neuromuscular disorder.

ARTERIAL PERIPHERAL PULSES

Simultaneous palpation of femoral and radial arteries r/o COA: femoral
< radial pulse
Fairly rapid rise to somewhat rounded peak
Anacrotic shoulder

Percussion wave
Incisura

AOP
CP

Tidal wave
Dicrotic wave

: aortic pressure
: internal carotid pulse

Anacrotic shoulder / ascending limb : peak of aortic flow before max.

pressure
Incisura: less steep downward deflection ; aortic closure
Peripheral : initial upstroke becomes steeper ; anacrotic shoulder
becomes less apparent ; incisura is replaced by a smoother dicrotic notch
More central pulse : more information : carotid pulse
Carotid pulse : sternocleidomastoid relaxed , head rotated towards the
examiner; press with thumb or forefinger
Trisection : sharpness of the upstroke , systolic peak and diastolic slope
Pulsus parvus : small weak pulse ; decreased LV SV, narrow pulse
pressure , increased peripheral vascular resistance ( PVR )
Hypokinetic pulse : hypovolemia, LV failure, restrictive, pericardial dses,
MV stenosis
Pulsus Tardus : delayed systolic peak , AV stenosis ; obstn. of LVEF
Hyperkinetic pulse : increased LV SV ;
wide pulse pressure ( > 40 mm Hg ; PP = SBP DBP ) :
Decreased in PVR ; complete heart block ,
hyperkinetic states ( anxiety, anemia , exercise, fever,
diastolic runoff like PDA and perip. AVF fistula ,
hyperthyroidism ),

due to vigorous LVEF : MR, VSD ( rapid upstroke,

decreased systolic duration & forward SV ) ; AR ( increased
LV SV & EF) Waterhammers sign
Bisferiens pulse : 2 systolic peaks ; AR and HOCM
HOCM : rises rapidly and forcefully producing the first systolic percussion
wave followed by a tidal wave
Dicrotic pulse : pulse 1 systole and 1 diastole ; very low SV in Dilated
CMP , cardiac tamponade , hypotension, and fever ( decreased
peripheral pressure ),
Pulsus alternans : regular alteration of the Pulse Pressure ( PP) amplitude
despite a regular rhythm ; severe functional impairment of LV with a loud
S3 ; paroxysmal tachycardia for several beats ffing a premature beat
Pulsus bigeminus : regular alteration of the PP amplitude ; Premature
Ventricular Contractions ( PVC) that follows each regular beat
Pulsus paradoxus : decrease in SBP > 10 mm Hg during inspiration ; the
peripheral pulse may disappear during inspiration ; pericardial tamponade ,
airway obstruction, or SVC obstruction

Inequality of pulses bet. carotid and radial arteries with right sided
pulses stronger supravalvular AS
Other causes of inequality : dissecting aneurysm, aortic arch
syndromes( atherosclerotic, syphilitic and arteritic), thoracic outlet
syndromes ( cervical rib, scaleneus anticus ) and local occlusive
disease of the peripheral artery
Other pulsations : right parasternal ( ascending aortic aneurysm) ;
Femoral and/or popliteal artery aneurysms should be sought in
patients with abdominal aortic aneurysm disease.
level of a claudication-producing arterial obstruction can often be
identified on physical examination
calf claudication, a decrease in pulse amplitude between the common
femoral and popliteal arteries will localize the obstruction to the level of
the superficial femoral artery, although inflow obstruction above the
level of the common femoral artery may coexist
However, the correlation between the presence of a bruit and the
degree of vascular obstruction is poor

cervical bruit is a weak indicator of the degree of carotid artery

stenosis; the absence of a bruit does not exclude the presence of
significant luminal obstruction
If a bruit extends into diastole or if a thrill is present, the obstruction is
generally severe

Peripheral Arterial disease : claudication, cool skin, abnormalities on

pulse examination, or the presence of a vascular bruit
Abnormal pulse oximetry (a >2% difference between finger and toe
oxygen saturation) can be used to detect lower extremity peripheral
arterial disease and is comparable in its performance characteristics to
the ankle-brachial index.

BLOOD PRESSURE
Brachial artery or radial artery ( upper extremities) and popliteal and
dorsalis pedis ( lower extremities )
Materials : BP apparatus with rubber cuff ( with the length encompassing
at least 80 to 100 % and width of 40 to 50% of the arm/ leg
circumference )
Seated for at least 15 mins ; 1 hr free from caffeine/ smoking ; BP cuff at
the level of the heart ; inflated rapidly to at least 30 mm Hg above the
obliteration of the pulse ( palpation method ) ; deflated slowly to around 3
mm Hg / sec, deflated rapidly after the DBP is noted
Auscultatory Method
Korotkoff sounds
phase 1 : clear tapping sounds ( SBP )
phase 2 : soft murmur
phase 3 : loud murmur ; blood flows to the constricted arteries
phase 4 : muffling sound ; constriction of the brachial artery
diminishes ( used in Pedia pts. )
phase 5 : disappearance of the sound ( DBP )
Normal : Phase 4 and 5 has a 10 mm Hg difference ( DBP )
chronic, severe AR or a large arteriovenous fistula because of enhanced
diastolic "run-off." DBP may be low or 0 mm Hg or if the difference of
phase 4 and phase 5 is > 10 mm Hg , one should measure phase 4 ( e.g.
BP = 142/ 54/ 10 mm Hg )
Auscultatory gap : implications : one may report a normal SBP when in
fact HPN is present ; technique : keep your finger on the pulsing artery as
you inflate the cuff until the pulse disappears then you know you are
above the SBP ; a silence that sometime separate the separates the first
appearance of the Korotkoff sounds from their second appearance at a
lower pressure ; venous distention or reduced velocity of arterial flow into
the arm ; seen in HPN, aortic valve dse., marked bradycardia and heart
failure
best assessed at the brachial artery level, though it can be measured at
the radial, popliteal, or pedal pulse level
Blood pressure should be measured in both arms, and the difference
should be less than 10 mmHg
Unequal BP on arms : atherosclerotic or inflammatory subclavian artery
disease, supravalvular aortic stenosis, aortic coarctation, or aortic
dissection.
Unequal pulse : take the BP of both upper and lower extremities
Normal : SBP legs up to 20 mm Hg higher than the arms but the DBP
identical
Hills sign : in AR ; SBP : popliteal > brachial artery by 20 mm Hg
Greater leg to arm pressure differences are seen in patients with chronic
severe AR as well as patients with extensive and calcified lower extremity
peripheral arterial disease

BP lower in lower extremities : coarctation of the aorta or obstructive

lesions of the aorta
ankle-brachial index (lower pressure in the dorsalis pedis or posterior tibial
artery divided by the higher of the two brachial artery pressures) is a
powerful predictor of long-term cardiovascular mortality.
"White coat hypertension" is defined by at least three separate clinicbased measurements >140/90 mmHg and at least two non-clinic-based
measurements <140/90 mmHg in the absence of any evidence of target
organ damage
Orthostatic hypotension : fall in systolic pressure >20 mmHg or in
diastolic pressure >10 mmHg in response to assumption of the upright
posture from a supine position within 3 min. There may also be a lack of a
compensatory tachycardia, an abnormal response that suggests
autonomic insufficiency, as may be seen in patients with diabetes or
Parkinson's
disease.
;
common
cause
of
postural
lightheadedness/syncope and should be assessed routinely ; exacerbated
by advanced age, dehydration, certain medications, food, deconditioning,
and ambient temperature.
Common Causes of inaccurate BP readings
Reading too low
Reading too high
Cuff too wide
- Cuff too narrow
Cuff bladder too short
- unusually fat arm
Unusually thin arm
- Patient discomfort
Too rapid deflation
Repeated readings
Overlooking auscultatory gap
Distended urinary bladder
Too firm pressure with stet

JUGULAR PULSE ( JVP)

single most important bedside measurement from which to estimate
the volume status.
internal jugular vein is preferred because the external jugular vein is
valved and not directly in line with the superior vena cava and right
atrium
Purpose : waveform and estimation of the CVP
Right internal JVP ; 30 degrees up to 90 degrees ; tangential light,
differentiate bet. Carotid arterial pulse ; phasic changes in the right
atrium
Best vein to use for estimation of CVP ( unit : cm of H2O ) ; 1.36 cm
H2O = 1 mm Hg
Sternal angle : reference point ; center of the RA lies approx. 5 cm
below the sternal angle regardless of body position
Vertical distance is less than 3 cm ( e.g. 3 cm + 5 cm= 8cm of blood )

Hepatojugular/ Abdominojugular reflux : palm over the abd. >10s

rise in JVP followed by a drop of > 4 cm blood upon release of firm
pressure ; indicative of RV failure due to increase LV filling pressure
Kussmauls sign : increase rather than the normal decrease in CVP
during inspiration ; severe RV HF, constrictive pericarditis or RV
infarction

Jugular venous pulse wave tracing (top) with heart sounds (bottom). The A wave represents
right atrial presystolic contraction and occurs just after the electrocardiographic P wave and just
before the first heart sound (I). In this example, the A wave is accentuated and larger than normal
due to decreased right ventricular compliance, as also suggested by the right-sided S4 (IV). The
C wave may reflect the carotid pulsation in the neck and/or an early systolic increase in right atrial
pressure as the right ventricle pushes the closed tricuspid valve into the right atrium. The x
descent follows the A wave just as atrial pressure continues to fall. The V wave represents atrial
filling during ventricular systole and peaks at the second heart sound (II). The y descent
corresponds to the fall in right atrial pressure after tricuspid valve opening. B. Jugular venous
wave forms in mild (middle) and severe (top) tricuspid regurgitation, compared with normal, with
phonocardiographic representation of the corresponding heart sounds below. With increasing
degrees of tricuspid regurgitation, the waveform becomes "ventricularized." C. ECG (top), jugular
venous waveform (middle), and heart sounds (bottom) in pericardial constriction. Note the
prominent and rapid y descent, corresponding in timing to the pericardial knock (K)

1. a wave : presystolic ; venous distention due to right atrial contraction ;

dominant wave
large a wave or Cannon a waves RA is contracting against a
strong resistance ( e.g. in TS) ; increased resistance to RV filling ( e.g.
in pulmo HPN, PS) ; RA contracts in a closed TV during RV systole
( e.g. in junctional rhythm, AV dissociation with V-tach or Complete
Heart Block )
absent a wave : atrial fibrillation ; first degree AV block
2. c wave : positive wave ; upward bulging of the TV during isovolumetric
systole and the impact of the carotid artery adjacent to the JV
3. x descent : atrial relaxation & downward displacement of the TV ;
accentuated : constrictive pericarditis
reduced : in RV dilation
reversed : in TR
4. v wave : positive, late systolic ; increasing volume in the RA while the
TV is closed ; during RV systole
Prominent : in TR
severe TR : prominent v wave and obliteration of the x descent
large systolic wave
5. y descent : opening of the TV; rapid inflow of blood into the RV
Rapid deep : severe TR, constrictive pericarditis, severe RV failure or
high venous pressure
Slow : obstruction to RV filling ; in TV stenosis, or RA myxoma

Differentiation between Jugular pulsation VS Carotid pulsation

INTERNAL JUGULAR PULSATIONS

Rarely palpable
Soft, rapid, undulating quality,
Usually w/ 2 elevations & 2 throughs
per heart beat
Pulsations eliminated by light pressure
On the vein (s) just above the sternal
End of the clavicle
Level of the pulsations changes w/
Position, dropping as the pt. becomes
More upright
Level of pulsations descends with inspiration

CAROTID PULSATIONS
- palpable
- a more vigorous thrust w/ a single
outward component
- Pulsations not eliminated by pressure

- Level of pulsations unchanged by

position
- Level of pulsations not affected
By inspiration

PRECORDIAL PALPATION
Location, amplitude , duration and direction of the cardiac impulse
fingertips
LV apex impulse : at or medial to the 4- 5th LMCL ICS ; less than 2.5 cm
in diameter ; best appreciated at end expiration , with the heart closer to
the anterior chest wall; note for size, amplitude and rate of amplitude
thin, tall patients and patients with advanced obstructive lung disease and
flattened diaphragms, the cardiac impulse may be visible in the
epigastrium and should be distinguished from a pulsatile liver edge
Supine, sitting ( leaning forward ) and left lateral decubitus
Enlargement of the LV cavity leftward and downward displacement of
an enlarged apex beat
LVH: increase in amplitude, duration, size of the LV thrust ; impulse
displaced laterally and downward into the 6th to 7th ICS ( AR and dilated
CMP )
sustained apex beat is a sign of pressure overload, such as that which
may be present in patients with AS or chronic hypertension

palpable presystolic impulse corresponds to the fourth heart sound (S4)

and is indicative of reduced left ventricular compliance and the forceful
contribution of atrial contraction to ventricular filling
palpable third sound (S3), which is indicative of a rapid early filling wave in
patients with heart failure, may be present even when the gallop itself is
not audible
HOCM : double systolic apical impulse ; may very rarely cause a triple
cadence beat at the apex with contributions from a palpable S 4 and the
two components of the bisferiens systolic pulse.
RVH : sustained systolic lift in the lower LPSB; synchronous with LV apical
impulse
Left ventricular dysynergy : myocardial infarction and during angina ; left
midprecordium 1 or 2 ICS &/or 1-2 cm medial t the LV apex
Severe MR : Left parasternal lift , synchronous with the v wave due to
anterior displacement of the RV because of an enlarged LA
Severe TR : right parasternal left ; enlarged RA
Pulsation of the Right sternoclavicular joint : right- sided aortic arch or
aneurysmal dilatation of the ascending aorta
Pulmonary artery pulsation : variable and palpable in the 2 nd L ICS ; may
be normal in children and thin young adults ; denotes pulmonary HPN;
increased pulmo. blood flow, or post-stenotic pulmonary arterial dilatation
Thrills : palpable , low frequency vibrations assoc. with heart murmurs ;
MR ( cardiac apex ) ; AS ( right side of the neck) ; PS ( left side of the
neck ) ; VSD ( 3rd to 4th ICS LPSBM )
Percussion : adds little information

CARDIAC AUSCULTATION:
Quiet room ; focus on the phase of the cardiac cycle ; timing of the
heart sound or murmur ( carotid arterial pulse, apical impulse or JVP),
cardiac sound or murmur (alterations, in its timing in physiologic and
pharmacologic interventions )
The eye and the ears often misses what is not in the observers mind ,
but sees and hears what it looks for . Didactic thinking
HEART SOUNDS :
vibrations assoc. with abrupt acceleration or deceleration of blood
FIRST HEART SOUND ( S1 ) : loudest at the apex ; closure of the
atrioventricular valves ( MV /TV )
influenced by the :
1. position of the mitral valve leaflet (MVL) at the onset of ventricular
systole
2. rate of rise of the LV pressure pulse
3. presence or absence of structural dse. of the MVL
4. amount of tissue , air or fluid between the heart and stethoscope

loud S1 : MS ( pliable and remains open in the onset of the

isovolumetric contraction because of elevated LA pressure )
soft S1 : poor conduction of sound through the chest wall, slow rise of
LV pressure pulse ( cardiomyopathy or systolic heart failure ), long PR
interval , or imperfect closure due to reduced valve substance ( mitral
regurgitation/ MR ) ; anterior MVL is immobile (severe and calcified
mitral stenosis/ MS )
; mechanical ventilation, obstructive lung
disease, obesity, pneumothorax, and a pericardial effusion.
Split S1 ( 10- 30 msec ) : normal ; Mitral Tricuspid closure
Widened S1 : CRBBB ; delay in the onset of RV pressure pulse
Reversed split S1 : TV MV closure ; severe MS , LA myxoma, LBBB

A. Normal. S1, first heart sound; S2, second heart sound; A2, aortic component of the second
heart sound; P2, pulmonic component of the second heart sound. B. Atrial septal defect with fixed
splitting of S2. C. Physiologic but wide splitting of S2 with right bundle branch block. D. Reversed
or paradoxical splitting of S2 with left bundle branch block. E. Narrow splitting of S2 with
pulmonary hypertension.

SECOND HEART SOUND

Loudest at the upper parasternal borders; closure of the semilunar valves
( aortic and pulmonic valves )
With normal or physiologic splitting, the A - P2 interval increases with
inspiration and narrows during expiration. This physiologic interval will
widen with right bundle branch block because of the further delay in
pulmonic valve closure and in patients with severe MR because of the
premature closure of the aortic valve

Split S2 : normal splits during inspiration ; A2 P2 closure ; best noted at

the RPSBM
RV increases in SV thus delay in closure of pulmonic valve
Types of split S2
1. Narrow split S2 :
a. Increase in Pulmonary vascular resistance ( PVR ) narrow split
S2 ( splitting that persists with expiration ( pulmonic area or LPSB )
2. Wide split S2 :
a. Delayed activation of the RV : RBBB , LV ectopic beats , LV
pacemaker,
b. Prolongation of the RV contraction w/ an increased RV pressure
overload : Pulmo. Embolism , PS
c. Early aortic valve closure : Constrictive pericarditis, MR and VSD
split S2 that persists even during expiration
3. Fixed split S2 :
a. RV volume overload ( RV failure or diminished impedance of the
pulmo. vasc. bed ) with prolonged hangout time: ASD
4. Reversed ( paradoxical splitting of S2 ) : delay in AV closure causing P2 to
precede A2 ; maximal during expiration and decreases during inspiration
a. Reversed split S2 : delayed excitation of the LV ( e.g. LBBB );
b. mechanical prolongation of the LV systole ( severe aortic outflow
obstruction/ AS , large aorta -pulmonary artery shunt , systolic
hypertension, IHD, cardiomyopathy )

Pulmo. Hypertension : loud P2 or single or narrow split S2 with palpable

P2
Normal : P2 < A2 or S2> S1 louder at : 2nd LICS ( base of the heart ) ;
and S1 > S2 at the apex
if S2 > S1 at the apex pulmonary HPN except ASD

SYSTOLIC SOUNDS :
Ejection sounds : sharp, high pitched; early systole, ffng the S1 ;
semilunar valve stenosis ( AS/ PS ), dilatation of the aorta or pulmo.
Artery ; heard at the LV apex area and 2 nd RICS
ejection sound that accompanies bicuspid aortic valve disease becomes
softer and then inaudible as the valve calcifies and becomes more rigid
Pulmonary Ejection sound : loudest ULSB ; heard better during expiration
ejection sound that accompanies pulmonic stenosis (PS) moves closer to
the first heart sound as the severity of the stenosis increases; the only
acoustic sound that decreases during inspiration
Non ejection clicks or midsystolic clicks with or without a late systolic
murmur : MVP or TVP ; result from chordae tendinae that are functionally
unequal in length or either or both AV valves ; heard at the LLSB and LV
apex

MVP : click-murmur complex will move away from the first heart sound
with maneuvers that increase ventricular preload, such as squatting. On
standing, the click and murmur move closer to S1.
Systolic clicks : later than the systolic ejection sound

DIASTOLIC SOUNDS
Opening snap ( OS ) : brief, high pitched , early diastolic sound, stenosis
of an AV valve ( MV/TV ) ;most often MV ;heard at LLSB and radiates to
the base of the heart ; decreases with progressive calcification and rigidity
of the anterior mitral leaflets
A2-OS interval ( 0.04 to 0.12 secs. ): inversely related to the height of the
mean left atrial pressure ; often confused with P2 at the 2 nd LICS
OS of TS occurs later in diastole than the mitral OS
Third heart sound ( S3 ) : low pitched ;produced in the ventricle ; 0.14 to
0. 16 s after A2 ; termination of the rapid filling ; rapid filling phase of
ventricular diastole; normal in children and pts with high cardiac output ;
over 40 y/o Ventricular failure / CHF ; disappears with tx of CHF
Left sided S3 : bell of stet; LV apex ; during expiration ; left lateral position
Right sided S3 : LSB or just beneath the xiphoid ; louder with inspiration ;
often accompanied with TR murmur
Early S3 (0.10 to 0. 12 s after A2 ) : constrictive pericarditis ; higher
pitched ( pericardial knock ) ; restrictive effect of the adherent pericardium
that abruptly halts the diastolic filling
Fourth Heart Sounds ( S4 ) : low pitched / bell of the stet ; presystolic
sound during ventricular filling ; effective atrial contraction; atrial filling
phase of ventricular diastole and indicates left ventricular presystolic
expansion ; absent in atrial fibrillation
S4 : diminished ventricular compliance
( diastolic dysfunction ) ;
resistance to ventricular filling ; seen in systemic hypertension, AS,
hypertrophic cardiomyopathy , IHD, acute MR, acute myocardial
infarction ; loud at LV apex, left lateral decubitus, increased in isotonic or
isometric exercise
Right sided S4 : RVH due to PS or pulmonary HPN ; frequently with
prominent systolic a wave in the JVP
S4 : delayed AV conduction ( AV blocks ) ; increases with age ; not
present with atrial fibrillation
pericardial knock (PK) is also high-pitched and occurs slightly later than
the opening snap, corresponding in timing to the abrupt cessation of
ventricular expansion after tricuspid valve opening and to an exaggerated
y descent seen in the jugular venous waveform in patients with
constrictive pericarditis
tumor plop is a lower-pitched sound that rarely can be heard in patients
with atrial myxoma. It may be appreciated only in certain positions and
arises from the diastolic prolapse of the tumor across the mitral valve

PART TWO LECTURE

HEART MURMURS :
vibrations of the heart , great vessels as a result of turbulent blood flow or
bubble formation due to sudden decrease in pressure
intensity , timing in the cardiac cycle , location and radiation, response to
various physiologic maneuvers
absence or presence of cardiac and noncardiac symptoms
Intensity :
Grade I so faint ; extra effort
Grade II audible on a quiet environment
Grade III readily audible
Grade IV with thrills ; loud
Grade V loud with rim of stet is raised off the chest ;thrill
Grade VI very loud even with stet removed from contact
with the chest ; thrill
Configuration
:
crescendo
,
decrescendo,
crescendodecrescendo( diamond shaped ) , or plateau

Principal Causes of Heart Murmurs

ORGANIC SYSTOLIC MURMURS
Midsystolic
Aortic
Obstructive
Supravalvular, supraaortic stenosis, coarctation of the aorta
Valvular AS and sclerosis
Subvalvular discrete or HOCM
Increased flow, hyperkinetic states, AR, complete heart block
Dilatation of ascending aorta, atheroma, aortitis, aneurysm of

aorta
Pulmonary
Obstructive
Supravalvular pulmonary arterial stenosis
Valvular pulmonic valve stenosis
Subvalvular infundibular stenosis
Increased flow, hyperkinetic states, left-to-right shunt (e.g., ASD,
VSD)
Dilatation of pulmonary artery
Holosystolic (regurgitant)
Atrioventricular valve regurgitation (MR, TR)
Left-to-right shunt at ventricular level (VSD)
EARLY DIASTOLIC MURMURS
Aortic regurgitation
Valvular; rheumatic deformity; perforation, postendocarditis,
posttraumatic, postvalvulotomy
Dilatation of valve ring: aorta dissection, annuloectasia, cystic
medial necrosis, hypertension
Widening of commissures: syphilis
Congenital: bicuspid valve, with VSD
Pulmonic regurgitation
Valvular: postvalvulotomy, endocarditis, rheumatic fever,
carcinoid
Dilatation of valve ring: pulmonary hypertension; Marfan
syndrome
Congenital: isolated or associated with tetralogy of Fallot, VSD,
pulmonic stenosis
MIDDIASTOLIC MURMURS
Mitral stenosis
Carey-Coombs murmur (middiastolic apical murmur in acute
rheumatic fever)
Increased flow across nonstenotic mitral valve (e.g., MR, VSD,
PDA, high-output states, and complete heart block)
Tricuspid stenosis
Increased flow across nonstenotic tricuspid valve (e.g., TR, ASD,
and anomalous pulmonary venous return)
Left and right atrial tumors
CONTINUOUS MURMURS
Patent ductus arteriosus
Coronary AV fistula
Ruptured aneurysm of sinus of Valsalva
Aortic septal defect
Cervical venous hum
Anomalous left coronary artery
Proximal coronary artery stenosis
Mammary souffle

Pulmonary artery branch stenosis

Bronchial collateral circulation
Small (restrictive) ASD with MS
Intercostal AV fistula
NOTE: AR, aortic regurgitation; AS, aortic stenosis; ASD, atrial
septal defect; AV, arteriovenous; HOCM, hypertrophic obstructive
cardiomyopathy; MR, mitral regurgitation; MS, mitral stenosis;
PDA, patent ductus arteriosus; TR, tricuspid regurgitation; VSD,
ventricular septal defect.

Effects of physiologic interventions:

Table 225-1. Effects of Physiologic and Pharmacologic Interventions on the
Intensity of Heart Murmurs and Sounds
Respiration Systolic murmurs due to TR or pulmonic blood flow through a normal
or stenotic valve and diastolic murmurs of TS or PR generally increase with
inspiration, as do right-sided S3 and S4. Left-sided murmurs and sounds usually
are louder during expiration.
Valsalva maneuver Most murmurs decrease in length and intensity. Two
exceptions are the systolic murmur of HCM, which usually becomes much louder,
and that of MVP, which becomes longer and often louder. Following release of the
Valsalva maneuver, right-sided murmurs tend to return to control intensity earlier
than left-sided murmurs.
After VPB or AF Murmurs originating at normal or stenotic semilunar valves
increase in the cardiac cycle following a VPB or in the cycle after a long cycle
length in AF. By contrast, systolic murmurs due to AV valve regurgitation either do
not change, diminish (papillary muscle dysfunction), or become shorter (MVP).
Positional changes With standing, most murmurs diminish, two exceptions being
the murmur of HCM, which becomes louder, and that of MVP, which lengthens
and often is intensified. With squatting, most murmurs become louder, but those
of HCM and MVP usually soften and may disappear. Passive leg raising usually
produces the same results.
Exercise Murmurs due to blood flow across normal or obstructed valves (e.g., PS,
MS) become louder with both isotonic and submaximal isometric (handgrip)
exercise. Murmurs of MR, VSD, and AR also increase with handgrip exercise.
However, the murmur of HCM often decreases with near maximum handgrip
exercise. Left-sided S4 and S3 are often accentuated by exercise, particularly
when due to ischemic heart disease.
Pharmacologic interventions During the initial relative hypotension following
amyl nitrite inhalation, murmurs of MR, VSD, and AR decrease, while murmurs of
aortic stenosis or sclerosis increase. During the later tachycardia phase, murmurs
of MS and right-sided lesions also increase. The response in MVP often is
biphasic (first softer and then louder than control). The arterial constrictor
phenylephrine tends to produce the opposite effects.
Transient arterial occlusion Transient external compression of both arms by

bilateral cuff inflation to 20 mmHg over peak systolic pressure augments the
murmurs of MR, VSD, and AR, but not murmurs due to other causes.
NOTE: TR, tricuspid regurgitation; TS, tricuspid stenosis; PR, pulmonic
regurgitation; HCM, hypertrophic cardiomyopathy; MVP, mitral valve prolapse; PS,
pulmonic stenosis; MS, mitral stenosis; MR, mitral regurgitation; VSD, ventricular
septal defect; AR, aortic regurgitation; VPB, ventricular premature beat; and AF,
atrial fibrillation.
SYSTOLIC MURMURS
Holosystolic ( Pansystolic ) murmurs : flow bet. 2 chambers that have
widely different pressures throughout systole (e.g. LA and LV ) ; begin with
S1 and ends with S2 ; MR / TR , VSD , aortopulmonary shunts
MR / VSD : augmented by exercise ; high pitched
TR : increases with inspiration ; assoc. with pulmo. HPN
Trivial MR : 45% of normal people ; Trivial TR by Doppler : 70% of normal
people ; PR in 88 %

MIDSYTOLIC MURMURS / SYSTOLIC EJECTION MURMURS :

Often crescendo-decrescendo ; across the aortic and pulmonary outflow
tract
Starts shortly after S1 ; as the semilunar valve opens and increases as
the velocity of the ejection increases and declines as the ejection
decreases ; murmur ends before the ventricular pressure falls enough to
permit closure of the AV and PV
Seen in pts with elevated cardiac output, ejection into a dilated vessel
beyond the valve ; increased transmission of sound through a thin chest
wall
Functional murmurs : benign ;2nd LICS ( pulmonary outflow tract ) ;
midsystolic

Valvular or subvalvar obstruction

Aortic stenosis : left sided ; midsystolic ; influenced by the direction of the
high velocity jet within the aortic root
Valvular AS : : 2nd RICS with radiation to the neck
Supravalvular AS : loudest even higher with disproportionate radiation to
the right carotid artery
HOCM : : originates in the LV cavity ; maximal at the LLPSB and apex
with relatively little radiation to the carotids
Highly calcified AS : soft and sometimes inaudible A2
MR/ TR ( from papillary muscle dysfunction / rupture chordae tendinae
inferior wall ischemia / infarction )
Normal : thin young ; high velocity of blood flow ; pulmonic area ; without
clinical significance
Louder murmur at the aortic area : young patients may indicate congenital
aortic stenosis
Elderly : aortic systolic murmurs > pulmonary flow murmurs ; due to
aortic dilatation , AS or to non stenotic thickening of the AV
Aortic and pulmonic murmurs : increased by amyl nitrite inhalation and
ffing a PVC
Aortic systolic murmurs : decreased by increased aortic impedance ;
transient arterial occlusion
EARLY SYSTOLIC MURMURS
Begin with S1 and ends in mid systole
Large VSD with pulmo. HPN
TR in the absence of pulmonary HPN narcotic abusers with IE ; large
right atrial v wave
Acute MR with a non compliant LA ; large v wave
LATE SYSTOLIC MURMUR
High pitched apical murmurs ; related to papillary muscle dysfunction due
to papillary muscle dysfunction ( infarction or ischemia ) or due to
distortion by left ventricular dilatation ; may transiently appear during
angina

Mid systolic click

( respectively )

ffed with a late systolic murmur MVP

with MR

Behavior of the click (C) and murmur (M) of mitral valve prolapse with changes in loading
(volume, impedance) and contractility. S1, first heart sound; S2, second heart sound. With
standing (left side of figure), volume and impedance decrease, as a result of which the click and
murmur move closer to S1. With squatting (right), the click and murmur move away from S1 owing
to the increases in left ventricular volume and impedance (afterload)

DIASTOLIC MURMUR
Early diastolic murmur : begin with or shortly after S2 ; soon as the
corresponding ventricular pressure falls below that in the aorta and the
pulmonary artery
AR : decrescendo ; diastolic blow ; high pitched ; LPSB with the patient
leaning forward ; expiration ; increased with hand grip ( acute elevation of
the arterial pressure ; diminishes with amyl nitrate inhalation ( decreased
in arterial pressure )
Congenital PR without pulmo. HPN : low to medium pitched ; early
diastolic murmur

MID DIASTOLIC MURMUR :

Usually arise from MV and TV ; during early ventricular filling ; quire loud
( grade III ) despite only slight AV valve stenosis, normal or increased
blood flow
Soft or absent despite severe obstruction if the CO is markedly reduced .
Marked AV stenosis : prolonged diastolic murmur ;

Index of severity of stenosis : duration is more reliable than the intensity

Low pitched MS : follows the OS

MS : bell ; apex ; left lateral decubitus ; increased by exercise and amyl

nitrite inhalation ; expiration
TS : LPSB ; inspiration
MR, PDA, VSD , TR or ASD rapid flow of blood across the AV valve
usually follow an S3 ; large left to right shunts or severe AV valve
regurgitation

Carey Coombs murmur - acute RF ; inflammation of the MV with

excessive LA blood flow ; with MR

Acute Severe AR : : LV diastolic pressure may exceed the LA pressure ;

mid diastolic murmur due to MR diastolic murmur of MR

Austin Flint Murmur of AR : chronic severe AR ; mid diastolic or pre

systolic ; originate at the anterior mitral valve leaflet when blood enters the
left ventricle simultaneously from the both the aortic root and the left
atrium

PRESYSTOLIC MURMUR
during ventricular filling that follows the atrial contraction ; in sinus rhythm
AV valve stenosis ( MS/ TS ); usually crescendo ; reaching peak intensity
at loud S1 ; at the moment of right and left atrial contraction
Right or left atrial myxoma : middiastolic or presystolic murmur

CONTINUOUS MURMUR
Begin in systole , peak near S2 and continue in all or part of diastole

Result from continuous flow due to communication between high- and

low- pressure areas ; persists through the end of systole and beginning of
diastole

PDA : continuous murmur as long as the pressure in the pulmonary

artery is below the aorta ; increased murmur by systemic arterial
hypertension and diastolic murmur may disappear by increased in
pulmonary arterial HPN leaving only the systolic murmur
Left to right shunt : Aortopulmonary septal defect , systemic arteriovenous
fistula, coronary arteriovenous fistula , anomalous origin of the LCA from
the PA ; communications between the Sinus of Valsalva and the right side
of the heart
Small ASD with high LA pressure
Pulmonary arteriovenous fistula : may be continuous but are usually only y
systolic
Disturbances of flow pattern : constricted systemic ( e.g. renal ) or
pulmonary arteries ; due to marked pressure differences between the 2
sides of the narrow segments
COA : continuous murmur in the back ; Pulmonary embolism : due to
partially occluded vessels

Rapid flow due to tortuous bed :

o bronchial artery collateral circulation in cyanotic pts. With severe
pulmonary outflow obstruction
o Mammary Souffle an innocent murmur heard over the breast
during late pregnancy and in the early postpartum due to increased
vasculature of the breast ; may be systolic or continuous
o Innocent cervical Hum medial aspect of the right supraclavicular
fossa ; patient in the upright position louder during diastole ;
abolished by digital compression of the right jugular vein ; may be
mistaken for PDA

PROSTHETIC HEART VALVES

mitral bioprosthesis usually is associated with a grade 2 or 3 midsystolic
murmur along the left sternal border (created by turbulence across the
valve struts as they project into the LV outflow tract) as well as by a soft
mid-diastolic murmur that occurs with normal LV filling During left
lateral decubitus and after exercise
high pitched or holosystolic apical murmur is indicative of paravalvular
leak or bioprosthetic regurgitation, for which additional imagining is
indicated
Bioprosthetic valve failure clinical deterioration

tissue valve in the aortic position is always associated with a grade 2 to 3

midsystolic murmur at the base or just below the suprasternal notch. A
diastolic ( high pitch ; blowing ; left parasternal border ) murmur of AR
may be noted
mechanical valve dysfunction - decrease in the intensity of either the
opening or the closing sound
high-pitched apical systolic murmur in patients with a mechanical mitral
prosthesis and a diastolic decrescendo murmur in patients with a
mechanical aortic prosthesis indicate paravalvular regurgitation
prosthetic valve thrombosis may present clinically with signs of shock,
muffled heart sounds, and soft murmurs.

PERICARDIAL FRICTION RUB:

Nearly 100 % specific for acute pericarditis however not sensitive
Leathery , scratchy components
3- or 2- or mono component : presystolic ( early rapid diastolic filling ),
systolic ( ventricular contraction) , and early diastolic filling;
may be confused for murmur or extracardiac sound esp. if heard only
during systole ; patient upright and leaning forward ; during inspiration
with ( in cardiac tamponade ) or without pulsus paradoxus

EXAMPLE OF NORMAL HEART PE and CVS PE:

- JVP= 5cm at 45 degrees
- Adynamic precordium, Apex beat visible and palpable at the 4th or 5th ICS
left midclavicular line ;(-) thrills / lift / heaves ; (-) loud and palpable P2 , S1
> S2 apex ; S2 > S1 at the base ; (-) S3 ; (-) S4 ; normal rate, regular
rhythm ; (-) murmurs
- Extremities : (-) clubbing and cyanosis ( -) varicose veins
- Pulses :
DP
PT
P
B
R
Right
++
++
++
++
++
Left
++
++
++
++
++
COMPLETE CARDIAC DIAGNOSIS :
Etiologic : Ischemic , congenital, hypertension, rheumatic , etc.
Anatomic : chambers dilated , structural defect ( e.g. stenosis, TOF , ASD,
VSD, etc. )
Physiologic : regurgitation, arrhythmias, pulmonary hypertension
Functional Classification :
New York Heart Classification :
I. No limitation
II. Mild limitation but can do ordinary activity
III. Moderate limitation but can do less than ordinary activity
IV. Severe limitation even at rest